World-class research involving neurodegenerative diseases such as Alzheimer's, and two other University of Otago brain research topics has been boosted by nearly $300,000 in nationally awarded grants.
Otago psychology department researcher Prof Cliff Abraham has received a grant of $201,384 to further his internationally leading Alzheimer's disease research, in the latest Neurological Foundation grant round.
Understanding the processes involved in neurodegenerative diseases such as Alzheimer's was critical in order to identify targets for drug therapies, foundation officials said.
The foundation's latest grant round amounted to about $1 million, bringing total research grants from the foundation to more than $40 million since the first foundation grants were allocated in 1972, foundation officials said.
Prof Abraham's project will investigate the role of astrocytes - non-neuronal brain cells - in controlling memory-related changes in the brain, and whether this regulation is impaired in a laboratory model of Alzheimer's disease.
Understanding this process could help to identify new targets for drug interventions to rescue impaired memory and cognition.
Learning occurs through changing the strength of synaptic connections between nerve cells in the brain.
Most neuronal cells communicate via synapses, and this process is impaired in neurological conditions such as Alzheimer's.
Otago anatomy department PhD student Laura Boddington gained a Neurological Foundation Postgraduate Scholarship, providing $84,000, to investigate whether a type of brain stimulation that uses the brain's own natural ''theta'' rhythms can improve recovery after someone suffers a stroke.
Recent Neurological Foundation-funded research using Theta Burst Stimulation (low-voltage electrical stimulation) had shown promise as a therapy for stroke victims.
Dr Julia Horsfield, of the Otago pathology department, gained $11,761 for a project investigating whether cohesin, a protein regulating cell division, influences the ability of a neuron to recognise itself, to avoid looping back on itself when connecting with other neurons, foundation officials said.
